Myelofibrosis
The latest news, research, and perspectives in myelofibrosis (MF). A primary subtype of myeloproliferative neoplasms (MPNs), this rare blood cancer scars the bone marrow so that it cannot properly produce blood cells.
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New or worsening anemia following initiation of ruxolitinib does not appear to diminish clinical benefit.
Hemoglobin improvement at week 24 after transfusion is associated with improved HRQOL in myelofibrosis and anemia.
Prospective analysis suggest that 4.3% of patients with ET progressed to myelofibrosis over five years of follow up.
Patients with MF or ET with CALR or JAK2 mutations carried similar symptom burdens according to prospective data.
The phase III MANIFEST-2 trial compared pelabresib plus ruxolitinib with placebo plus ruxolitinib in JAKi-naive patients.
The findings were from a retrospective study of patient data from the US Flatiron Health electronic health record database.
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A retrospective analysis covered two phase III trials of the JAK2 inhibitor in patients with and without monocytosis.
A study evaluated progression according to hemoglobin levels, platelet counts, constitutional symptoms, and other markers.
CTLA-4 blockade increased the cytotoxic T-cell–mediated immune response against myelofibrosis cells in human xenografts.
A Markov model has compared delayed with immediate performance of allogeneic HSCT following ruxolitinib failure in PMF.
Using mass spectrometry-based proteomics, chemokine platelet factor 4 (PF4) was identified as a driver of myelofibrosis.
New therapies, such as TP-3654, are currently being explored in combination studies.
Three of four patients with myelofibrosis had objective responses at one year, and no dose-limiting toxicities were observed.
No significant differences in HSCT were observed, suggesting haploidentical HSCT as an acceptable treatment approach.
AI-driven quantitative analysis was compared with manual evaluation of bone marrow trephine slides in a phase II trial.
Julie Braish, MBBCh, discusses her study on JAK2 allele burden in myelofibrosis presented at ASCO 2024.
Dr. Rampal, of Memorial Sloan Kettering Cancer Center, discusses his abstract at the EHA 2024 Congress in Madrid, Spain.
MPN depend on mutated JAK signaling, and targeting the mutations suppressed disease features and improved overall survival.
Pelabresib plus ruxolitinib improved spleen and symptom responses in JAKi-naïve patients with myelofibrosis.
Treatment with luspatercept improved transfusion burden and anemia across four cohorts of patients with myelofibrosis.
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Editorial Board
Sagar Lonial, MD, FACPEditor-in-Chief | Chief Medical Officer of Winship Cancer Institute at Emory University School of Medicine
Guillermo Garcia-Manero, MDAssociate Editor | Chief, Section of Myelodysplastic Syndromes, The University of Texas MD Anderson Cancer Center
Elias Jabbour, MDExecutive Editor | DB Lane Cancer Research Fund Distinguished Professor in Leukemia Research, MD Anderson Cancer Center
Kami Maddocks, MDAssociate Editor | Professor of Clinical Internal Medicine in the Division of Hematology at The Ohio State University
Thomas Martin, MDAssociate Editor | Clinical Research Director, UCSF Helen Diller Family Comprehensive Cancer Center
Jerald Radich, MDAssociate Editor | Professor in the Clinical Research Division and Kurt Enslein Endowed Chair at Fred Hutch
Laurie Sehn, MD, MPHAssociate Editor | Clinical Professor of Medical Oncology, British Columbia Cancer Centre for Lymphoid Cancer
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